Villagers of Bukit Koman in Raub today failed in their bid to stop a goldmine from carrying out its activities which were causing environmental damages and health concerns.

Dari Tukar tiub :

KESIAN ORANG KAMPUNG BUKIT KOMAN

Montana , The Czech Republic has banned the use of cyanide in mining, and both Turkey and Greece have made significant court rulings against issuing permits to mining interests whose projects propose the use of cyanide. The Mining Amendment (Cyanide Leaching) Bill 2000, which would prohibit ore processing by cyanide leaching in gold mining, was entered into the Parliament in New South Wales, Australia, in June 2000.FEBRUARY 2009Raub Australian Gold Mining Sdn. Bhd. started the mining process with Cyanide. Residents started to notice stinging smell. Since then, many residents started to experience insomnia, vomiting, dizziness and other abnormal symptoms. The total number of report of abnormal symptoms has rose to more than 200 cases.

Info dari Wikipedia :

Acute poisoning

Cyanide makes the cells of an organism unable to use oxygen. Inhalation of high concentrations of cyanide causes a coma with seizures, apnea and cardiac arrest, with death following in a matter of minutes. At lower doses, loss of consciousness may be preceded by general weakness, giddiness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the victim progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. Skin color goes pink from cyanide-hemoglobin complexes. A fatal dose for human can be as low as 1.5mg/kg body weight[1]Chronic exposureExposure to lower levels of cyanide over a long period (e.g., after use of cassava roots as a primary food source in tropical Africa) results in increased blood cyanide levels, which can result in weakness and a variety of symptoms, including permanent paralysis.Treatment of poisoning and antidotesThe United States standard cyanide antidote kit first uses a small inhaled dose of amyl nitrite, followed by intravenous sodium nitrite, followed by intravenous sodium thiosulfate.[citation needed] Alternative methods of treating cyanide intoxication are used in other countries.

Agent & Description :

nitrites and sodium thiosulfateThe nitrites oxidize some of the hemoglobin's iron from the ferrous state to the ferric state, converting the hemoglobin into methemoglobin. (Treatment with nitrites is not innocuous as methemoglobin cannot carry oxygen). Cyanide preferentially bonds to methemoglobin rather than the cytochrome oxidase, converting methemoglobin into cyanmethemoglobin.[citation needed] In the last step, the intravenous sodium thiosulfate converts the cyanmethemoglobin to thiocyanate, sulfite, and hemoglobin. The thiocyanate is excreted.

hydroxycobalaminIn France, hydroxycobalamin (a form of vitamin B12) is used to bind cyanide to form the harmless vitamin B12a cyanocobalamin. Cyanocobalamin is eliminated through the urine. Hydroxycobalamin works both within the intravascular space and within the cells to combat cyanide intoxication. This versatility contrasts with methemoglobin, which acts only within the vascular space as an antidote. Administration of sodium thiosulfate improves the ability of the hydroxycobalamin to detoxify cyanide poisoning. This treatment is considered so effective and innocuous that it is administered routinely in Paris to victims of smoke inhalation to detoxify any associated cyanide intoxication. However it is relatively expensive and not universally available

4-Dimethylaminophenol4-Dimethylaminophenol (4-DMAP) has been proposed in Germany as a more rapid antidote than nitrites with (reportedly) lower toxicity. 4-DMAP is used currently by the German military and by the civilian population. In humans, intravenous injection of 3 mg/kg of 4-DMAP produces 35 percent methemoglobin levels within 1 minute. Reportedly, 4-DMAP is part of the US Cyanokit, while it is not part of the German Cyanokit due to side effects (e. g. hemolysis).

dicobalt edetateCobaltsalts have also been demonstrated as effective in binding cyanide. One current cobalt-based antidote available in Europe is dicobalt edetate or dicobalt-EDTA, sold as Kelocyanor. This agent chelates cyanide as the cobalticyanide. This drug provides an antidote effect more quickly than formation of methemoglobin, but a clear superiority to methemoglobin formation has not been demonstrated. Cobalt complexes are quite toxic, and there have been accidents reported in the UK where patients have been given dicobalt-EDTA by mistake based on a false diagnoses of cyanide poisoning.

glucoseEvidence from animal experiments suggests that coadministration of glucose protects against cobalt toxicity associated with the antidote agent dicobalt edetate. For this reason, glucose is often administered alongside this agent (e.g. in the formulation 'Kelocyanor').It has also been anecdotally suggested that glucose is itself an effective counteragent to cyanide, reacting with it to form less toxic compounds that can be eliminated by the body. One theory on the apparent immunity of Grigory Rasputin to cyanide was that his killers put the poison in sweet pastries and madeira wine, both of which are rich in sugar; thus, Rasputin would have been administered the poison together with massive quantities of antidote. One study found a reduction in cyanide toxicity in mice when the cyanide was first mixed with glucose[1]. However, as yet glucose on its own is not an officially acknowledged antidote to cyanide poisoning.

3-Mercaptopyruvate prodrugsAntidotes for the therapeutic management of cyanide poisoning, especially in the U.S., have relied mainly on the enzyme rhodanese (thiosulfate/cyanide sulfurtransferase, EC 2.8.1.1) for detoxification. This enzyme uses thiosulfate to form an activated-sulfane complex, which reacts with cyanide to form the less-toxic thiocyanate, that is excreted in the urine. Rhodanase is concentrated in the liver and kidneys where it is found in the mitochondrial matrix, a site of low accessibility for ionized, inorganic species, such as thiosulfate. This compartmentation of rhodanase in mammalian tissues leaves major targets of cyanide lethality, namely, the heart and central nervous system unprotected. (Rhodanase is also found in red blood cells, but its relative function has not been clarified.[2][3]

Researchers at the University of Minnesota are exploiting a different cyanide metabolic pathway in their antidote program: 3-mercaptopyruvate sulfur transferase (3-MPST, EC 2.8.1.2) which is more widely distributed in mammalian tissues than rhodanase. Analogous to rhodanase, 3-MPST uses its substrate to convert cyanide to thiocyanate, but instead of thiosulfate, the natural substrate of 3-MPST is the cysteine catabolite, 3-mercaptopyruvate (3-MP). However, 3-MP is chemically unstable, and attempts at intravenous administration to counteract the toxicity of cyanide have been unsuccessful due to this instability. The Minnesota researchers have therefore developed an effective prodrug of 3-mercaptopyruvate that, when administered orally or parenterally, forms 3-MP. These cyanide antidotes are under advanced preclinical evaluation at the University of Minnesota[4][5][6]

Oxygen therapyOxygen therapy is not a cure in its own right, however the human liver is very capable of metabolizing cyanide very quickly (smokers breathe in hydrogen cyanide, but it is metabolized so fast that it does not accumulate or have any effect). Therefore if the patient can be kept comfortable with just oxygen alone, then the liver can be left to destroy the cyanide. This has the advantage that no chemicals are administrated, which might have an adverse effect.The International Programme on Chemical Safety issued a survey (IPCS/CEC Evaluation of Antidotes Series) that lists the following antidotal agents and their effects: Oxygen, sodium thiosulfate, amyl nitrite, sodium nitrite, 4-dimethylaminophenol, hydroxocobalamin, and dicobalt edetate ('Kelocyanor'), as well as several others[2]. Other commonly-recommended antidotes are 'solutions A and B' (a solution of ferrous sulfate in aqueous citric acid, and aqueous sodium carbonate) and amyl nitrite.

The UK Health and Safety Executive (HSE) has recommended against the use of solutions A and B because of their limited shelf life, potential to cause iron poisoning, and limited applicability (effective only in cases of cyanide ingestion, whereas the main modes of poisoning are inhalation and skin contact). The HSE has also questioned the usefulness of amyl nitrite due to storage/availability problems, risk of abuse, and lack of evidence of significant benefits. It also states that the availability of Kelocyanor at the workplace may mislead doctors into treating a patient for cyanide poisoning when this is an erroneous diagnosis. The HSE no longer recommends a particular cyanide antidote.[7] Qualified UK first aiders are now only permitted to apply oxygen therapy using a bag valve mask, providing they have been trained in its usage.